Effect of Inhalation Injury on Lung Water Accumulation
- 1 July 1983
- journal article
- research article
- Published by Wolters Kluwer Health
- Vol. 23 (7) , 597-604
- https://doi.org/10.1097/00005373-198307000-00009
Abstract
Thermally injured patients (14) with severe inhalation injury were sequentially studied with the thermal-green dye double indicator dilution technique of extravascular lung water (EVLW) measurement. Eight females and 6 males (average age, 49 yr, and average thermal burn, 37% body surface) were studied for 2-31 days postinjury. All were burned in a closed space, had facial burns, soot in their sputum, and a mean HbC level of 30%. Nine patients died, 6 of sepsis, 1 each of acute renal failure, hepatorenal syndrome and anoxic brain damage. Mean EVLW on admission was 7.0 .+-. 2.9 ml/kg and remained normal in the 5 survivors and in the patients dying of acute renal failure and anoxic brain damage. Six patients had increases in EVLW, caused by altered pulmonary capillary permeability in 5 and by elevation of hydrostatic pressures in 1 patient (hepatorenal death). Of the 5 patients with permeability edema, 1 appeared to result from a direct early effect of inhalation injury resulting in an EVLW of 13.3 ml/kg on admission. The other 4 patients had EVLW increases after the onset of sepsis, resulting in a mean EVLW of 23.2 .+-. 7.2 ml/kg at death (P < 0.01). Of all patients 71% developed pneumonia, which appears to have caused an EVLW increase in 1 patient; the other EVLW increases were caused by systemic sepsis. In a study of 14 patients with definite severe inhalation injury only 1 had an early increase in EVLW directly related to the inhalation injury, an early effect on capillary permeability presumably caused by direct chemical toxicity of inhaled gases. The remaining 4 cases of permeability edema occurred 4-24 days postinjury and resulted from burn wound or pulmonary sepsis. Increases in EVLW after thermal and inhalational injury are primarily caused by systemic or pulmonary sepsis, and have a delayed onset. Early increases in EVLW may be a result of the chemical toxicity of inhaled gases but are very uncommon, moderate in degree, and are seen only with the severest cases of inhalation injury.This publication has 6 references indexed in Scilit:
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